Cancers are now responsible for one third of deaths in Japan, and it is therefore an urgent problem to establish therapeutic means appropriate for cancers. In multiple myeloma, the therapeutic environment is now being improved by introduction of lenalidomide and bortezomib (i.e., a specific inhibitor of proteasomes). On the other hand, however, there are numerous cases where cancer cells have acquired resistance to existing drugs, thereby causing recurrence. For this reason, there has been a need to develop an anticancer agent having a different mechanism of action from conventional drugs. Further, such an anticancer agent can be used in combination with existing therapies if they differ in their dose limiting toxicity (DLT), which allows planning of a more effective therapeutic strategy.
EGCG (epigallocatechin gallate, epigallocatechin-O-gallate), which is one of the major catechins contained in green tea, has been reported to have an anticancer effect (Non-patent Document 1), and a phase II clinical trial has been conducted in patients with chronic lymphocytic leukemia, a type of blood cancer (Non-patent Document 2). In our previous reports, we have elucidated that EGCG exerts an anticancer effect upon binding to its target molecule 67-kDa laminin receptor (67LR) on the cell membrane (Non-patent Documents 3 to 6). This 67LR has been initially found as a protein binding to laminin, a member constituting the basement membrane (Non-patent Document 7). In recent studies, 67LR has been found to show abnormally enhanced expression in cancer cells (Non-patent Document 8), and a strong correlation has been found between 67LR expression and invasion or metastasis (Non-patent Documents 9 to 15). EGCG has been reported to selectively kill only leukemia cells or multiple myeloma cells via the 67LR-mediated mechanism (Non-patent Documents 16 and 17), thus suggesting that EGCG can serve as a molecular targeted agent against 67LR-positive leukemia cells or multiple myeloma cells. However, the lethal effect of EGCG on leukemia cells or multiple myeloma cells is limited (Non-patent Document 2), and hence there has been a strong demand for enhancement of the effect when EGCG is used as an anticancer agent.